1. The highly oncogenic endogenous viruses of mouse origin have been demonstrated to be derived by the mechanism of genetic recombination in the env gene. This recombinational event leads to acquisition of a unique common class of envelope glycoprotein determinants by different ecotropic viruses which are presumably required for oncogenicity. 2. The type C and type D retroviruses of primate origin were shown to recognize common cellular receptor site for infection process as determined by in vitro binding of glycoprotein to the cells in culture. These finding suggest that either type D and type C viruses of primate origin have required common env gene sequences for receptor site recognition by genetic recombination or alternatively the sequences involved in receptor site recognition are evolutionarily conserved and share common progenitor. 3. Several non-conditional replication defective mutants of type C viruses of primate origin and a type D virus were isolated. These mutants were shown to be defective in post-translational processing of gag gene coded structural proteins. The identification and immunologic characterization of each of the intermediate cleavage products led to tentative deduction of intracistronic order of individual structural proteins within SMRV gene precursor as NH2-p16-p12-p30-p9-COOH.